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目的:观察他汀对冠心病患者内皮祖细胞(EPCs)增殖力的影响及与PI3/Akt和ERK信号通道的相关性。方法:冠心病和非冠心病患者各16例纳入实验,非冠心病患者的10mL外周血来源的单个核细胞纳入正常组,冠心病患者的40mL外周血来源的单个核细胞均分纳入10μmol/L阿托伐他汀组、10μmol/L阿托伐他汀+PI3/Akt通道阻滞剂LY294002组和10μmol/L阿托伐他汀+ERK信号通道阻滞剂PD98059组,均向EPCs方向分化,以VEGFR2、CD34和AC133流式鉴定;观察冠心病患者EPCs增殖力的变化及他汀的影响,观察LY294002和PD98059分别阻断PI3/Akt和ERK通道后他汀对冠心病患者EPCs增殖力作用的变化。结果:与非冠心病人对比,冠心病患者EPCs的增殖(0.23±0.02 to 0.14±0.02,P<0.001)功能下降,阿托伐他汀明显提高冠心病患者EPCs的增殖力(0.14±0.02 to 0.20±0.02,P<0.05);该作用可为PI3/Akt通道阻滞剂LY294002阻断(0.20±0.02 to 0.16±0.02,P<0.001),但ERK信号通道阻滞剂PD98059无此作用(0.20±0.02比0.20±0.02,P>0.05)。结论:阿托伐他汀可通过PI3/Akt通道而非ERK信号通道上调冠心病患者外周血来源EPCs的增殖力。
Objective: To observe the effects of statins on the proliferation of endothelial progenitor cells (EPCs) and the relationship with PI3 / Akt and ERK signaling pathway in patients with coronary heart disease. Methods: Sixteen patients with coronary heart disease and non-coronary heart disease were enrolled in the experiment. Ten mL of peripheral blood mononuclear cells from non-patients with coronary heart disease were included in the normal group. Peripheral blood mononuclear cells (40 mL) from patients with coronary heart disease were included in 10 micromol / L Atorvastatin group, 10μmol / L atorvastatin + PI3 / Akt channel blocker LY294002 group and 10μmol / L atorvastatin + ERK signal pathway blocker PD98059 group all differentiated into EPCs, VEGFR2, CD34 and AC133. The changes of EPCs proliferation in patients with CHD and the effect of statins were observed. The changes of EPCs proliferation in patients with CHD after LY294002 and PD98059 were blocked by PI3 / Akt and ERK channels respectively were observed. Results: The proliferation of EPCs in patients with coronary heart disease (0.23 ± 0.02 to 0.14 ± 0.02, P <0.001) decreased compared with non-coronary patients, and atorvastatin significantly increased the proliferation of EPCs in patients with coronary heart disease (0.14 ± 0.02 to 0.20 ± 0.02, P <0.05). This effect was blocked by PI3 / Akt channel blocker LY294002 (0.20 ± 0.02 to 0.16 ± 0.02, P <0.001), but ERK signal pathway blocker PD98059 had no effect 0.02 vs. 0.20 ± 0.02, P> 0.05). Conclusion: Atorvastatin can up-regulate the proliferation of peripheral blood-derived EPCs in patients with coronary heart disease through the PI3 / Akt pathway but not the ERK signaling pathway.